Effects Of MIBG On Proliferation In Hepatoma Carcinoma HepG2Cells

Objective: To study the effects of inhibitor of arginine-specificmono-ADP-ribosylation MIBG(meta-iodobenzylguanidine) on proliferationin hepatoma carcinoma HepG2cells and its possible mechanism.Methods:1The expression of ART1in HepG2cells was detected bycellular immunofluorescence method.2The effect of different concentration of MIBG on cell survival ratewere measured by MTT assay3The effect of different concentration of MIBG on cell cycle phases inHepG2cells were measured flow cytometry.4The expression of ART1, RhoA,c-myc and cyclin A1were detectedby Western blot.Results:1Immunofluores: It showed that the ART1expressed in theHepG2cells, compared with the negative group.2MTT assay: We found that the MIBG could inhibit the growth of theHepG2cells,which could be affected by different concentrations (P<0.05).3Flow cytometry: With the concentration of the MIBG increasing,the percentage of the cells in S phase increased correspondingly (P<0.05). The growth of the HepgG2cells was arrested by MIBG in S phase.4Western blot: The expression of the ART1, RhoA, c-myc andcyclinA1decreased after using the MIBG (P<0.05). The expression of theART1,RhoA,c-myc and cyclinA1were lower in the150μmol/L group thanthe50μmol/L group (P<0.05).Conclusion: The MIBG could inhibit the proliferation of HepG2cells.The mechanism could be that the effect of mono-ADP-ribosylation wasweakened after using the MIBG.Then, the expression of c-myc andcyclinA1decreased, because the activation of the RhoA decreased. Finally,the HepG2cells were arrested in S phase, which the growth of HepG2cellswas inhibited.